The RECQL helicase prevents replication fork collapse during replication stress

Bente Benedict, Marit Ae van Bueren, Frank Pa van Gemert, Cor Lieftink, Sergi Guerrero Llobet, Marcel Atm van Vugt, Roderick L Beijersbergen, Hein Te Riele*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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Most tumors lack the G1/S phase checkpoint and are insensitive to antigrowth signals. Loss of G1/S control can severely perturb DNA replication as revealed by slow replication fork progression and frequent replication fork stalling. Cancer cells may thus rely on specific pathways that mitigate the deleterious consequences of replication stress. To identify vulnerabilities of cells suffering from replication stress, we performed an shRNA-based genetic screen. We report that the RECQL helicase is specifically essential in replication stress conditions and protects stalled replication forks against MRE11-dependent double strand break (DSB) formation. In line with these findings, knockdown of RECQL in different cancer cells increased the level of DNA DSBs. Thus, RECQL plays a critical role in sustaining DNA synthesis under conditions of replication stress and as such may represent a target for cancer therapy.

Original languageEnglish
Article numbere202000668
Number of pages14
JournalLife science alliance
Issue number10
Publication statusPublished - 20-Aug-2020

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